ReviewCell death and differentiation2026
Cardiac fibroblast Foxm1 deficiency prevents pressure overload-induced cardiac remodeling via the Usp10/MKK6-p38γ MAPK axis.
Review in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- ZEB2 SUMOylation in Cardiac Fibroblast Drives Post-Infarction Cardiac Remodeling through CtBP1-Associated repression of Nr4a1.iScience · 2026Article
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- Sennoside A Ameliorates Myocardial Fibrosis After Myocardial Infarction by Binding to KDM4B and Regulates IRX2 Expression.Cardiovascular drugs and therapy · 2026Article
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
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Authors and funding
18 authors.
Funding
Abstract
Cardiac fibroblasts (CFs) activation plays a crucial role in cardiac remodeling. However, the molecular mechanisms underlying the fibroblast-to-myofibroblast transition remain largely unknown. Here we found elevated Foxm1 expression in human heart failure (HF) samples as well as in the mouse cardiac remodeling model. CFs were the primary cell type responsible for Foxm1 upregulation. Foxm1 genetic knockout in CFs or myofibroblasts significantly attenuated TAC-induced cardiac remodeling and HF. Conversely, conditional overexpression of Foxm1 in CFs resulted in more severe pathological cardiac remodeling and dysfunction by TAC. Combined RNA-sequencing and MS analysis revealed that Foxm1 promoted p38 mitogen-activated protein kinase (MAPK) signalling pathway. Mechanically, Foxm1 not only upregulates USP10 to reduce the ubiquitination and degradation of p38γ but also directly drives the expression of MKK6 to increase the phosphorylation levels of p38, thereby acting as a dual amplifier for p38 activation. Genetic knockout of p38γ ameliorated the exacerbated TAC-induced cardiac remodeling in mice with Foxm1 overexpression in CFs. Our findings suggest that targeting the Foxm1-USP10/MKK6-p38γ MAPK axis may represent a new potential therapeutic strategy against pathological cardiac remodeling and HF. Foxm1 promotes the CFs activation during TAC-induced pathological cardiac remodeling through modulation of the USP10/MKK6-p38γ MAPK signalling pathway. Pro-fibrotic stimuli increase Foxm1 expression, which upregulates USP10 to reduce the ubiquitination and degradation of p38γ but also directly drives the expression of MKK6 to increase the phosphorylation levels of p38, thereby acting as a dual amplifier for p38 activation and promoting fibroblast-to-myofibroblast transition. Moreover, genetic knockout of p38γ mitigates exacerbated TAC-induced pathological cardiac remodeling in mice with Foxm1 overexpression in CFs.
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